Our research goal is to understand the molecular and cellular mechanisms underlying normal development and degenerative retinal diseases, and to establish the intervening strategies. Topics we currently study include: (I) Functional analysis of apical polarity gene Pals1 during retinal and lens development, (II) Pathophysiological study of degenerative retinal diseases, LCA (Leber Congenital Amaurosis) and RP (Retinitis Pigmentosa), to understand disease-causing mechanisms. We are particularly interested in polarity defects in retinal progenitor cells, which cause early-onset, photoreceptor degeneration in LCA type 8, (III) Cell-transplantation and gene-based therapies to to restore vision loss in LCA8-like mouse models in animal settings, (IV) Investigating the function of tumor suppressor-oncogene signal transduction pathways, TSC2-mTOR and Hippo-Yap, in eye development. Fundamental questions that we are trying to answer through these studies include, but are not limited to: (1) How is organ size determined? How are cellular contact inhibition signals translated and coordinated to cell proliferation activity in the nucleus? (2) How is cell size determined? How are differential cell sizes achieved and maintained? (3) What are the functions of the apical polarity complex during CNS development? (4) Can visual impairment in degenerative retinal diseases be rescued by gene- or cell-based therapies? Currently, we are using a combination of molecular and cellular methods, high-throughput (microarray), imaging (including confocal and multi-photon) and mouse genetics approaches (including conditional knock-out technology).